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Autoimmune drug may help prevent kidney disease caused by diabetes

Date:

March 27, 2014

Source:

American Society of Nephrology (ASN)

Summary:

A receptor called B7-1 is expressed by kidney cells during the progression of kidney disease in diabetic mice and humans. Targeting this receptor with an available drug called CTLA4-Ig, or abatacept, helps to maintain kidney function in mice, research concludes. "The next steps will be to test anti-B7-1 drugs in individuals with diabetes and diabetic nephropathy to see if they can abrogate the progression of the disease in humans as well," said a lead author.

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A drug currently used to treat autoimmune disease may also help prevent the kidney-damaging effects of diabetes, according to a study appearing in an upcoming issue of the Journal of the American Society of Nephrology (JASN). The findings suggest that clinical trials should be designed to test the drug in diabetic patients.

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Kidney disease is one of the most serious complications of diabetes. Diabetics who develop kidney disease, or diabetic nephropathy, due to high blood glucose levels may eventually require dialysis or a kidney transplant.

Paolo Fiorina, MD, PhD (Boston Children's Hospital/Harvard Medical School) and his colleagues have discovered that a receptor called B7-1 is expressed by kidney cells during the progression of diabetic nephropathy. Furthermore, targeting this receptor with an available drug called CTLA4-Ig, or abatacept, helped to maintain kidney function in mice with diabetic nephropathy. Abatacept is currently being used to treat autoimmune disease due to its ability to target B7-1 expressed on immune cells.

"The next steps will be to test anti-B7-1 drugs in individuals with diabetes and diabetic nephropathy to see if they can abrogate the progression of the disease in humans as well," said Dr. Fiorina.

American Society of Nephrology (ASN). (2014, March 27). Autoimmune drug may help prevent kidney disease caused by diabetes. ScienceDaily. Retrieved March 3, 2015 from www.sciencedaily.com/releases/2014/03/140327222206.htm

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